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• W2097252258 endingPage "2960" @default.
• W2097252258 startingPage "2951" @default.
• W2097252258 abstract "Thiamin-responsive megaloblastic anemia syndrome (TRMA) is characterized by diabetes mellitus, megaloblastic anemia and sensorineural deafness. Mutations in the thiamin transporter gene SLC19A2 cause TRMA. To generate a mouse model of TRMA, we developed an Slc19a2 targeting construct using transposon-mediated mutagenesis and disrupted the gene through homologous recombination in embryonic stem cells. Erythrocytes from Slc19a2−/− mice lacked the high-affinity component of thiamin transport. On a thiamin-free diet, Slc19a2−/− mice developed diabetes mellitus with reduced insulin secretion and an enhanced response to insulin. The diabetes mellitus resolved after 6 weeks of thiamin repletion. Auditory-evoked brainstem response thresholds were markedly elevated in Slc19a2−/− mice on a thiamin-free diet, but were normal in wild-type mice treated on that diet as well as thiamin-fed Slc19a2−/− mice. Bone marrows from thiamin-deficient Slc19a2−/− mice were abnormal, with a megaloblastosis affecting the erythroid, myeloid and megakaryocyte lines. Thus, Slc19a2−/− mice have provided new insights into the TRMA disease pathogenesis and will provide a tool for studying the role of thiamin homeostasis in diabetes mellitus more broadly." @default.
• W2097252258 created "2016-06-24" @default.
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• W2097252258 date "2002-11-01" @default.
• W2097252258 modified "2023-10-01" @default.
• W2097252258 title "Targeted disruption of Slc19a2, the gene encoding the high-affinity thiamin transporter Thtr-1, causes diabetes mellitus, sensorineural deafness and megaloblastosis in mice" @default.
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• W2097252258 doi "https://doi.org/10.1093/hmg/11.23.2951" @default.
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